90,767 research outputs found

    The political role of the people's liberation army 1949-1973

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    This thesis is to study the political role of the People's Liberation Army from the approach of structure and function. The framework of the thesis consists of three major parts, first, the influence of Chinese traditional political culture on, and the formation of, the political role of the PL A; second, the influence of domestic political struggles and external military conflicts on the development of the political role of the PLA; and the third, the analysis of the transition of the PLA's political role from the structure and personnel arrangements of the CCPCC Within the above-mentioned three scopes, this thesis make a thorough discussion on the following: (1) The relationship between the structure of the PRC and the formation of the PLA's political role; (2) How has ideology influenced the army's political role; (3) What is Mao's viewpoint and his influence on the development of the army's political role; (4) What is the link between the army and the party, and how has this developed; (6) What accounts for the expansion of the PLA's political functions; (7) What is the influence of political factional struggles on the PLA's political role; (8) Is it political institution or military institution that controls the recruitment of the military elite; (9) What are the disparities between the military elite in handling international conflicts and what are their political considerations; (10) What is the Party's position in the army; (11) How have the Party’s important meetings and personnel arrangements influenced the rise and fall of the PLA's political role

    The expression of p53 and PTTG1 in oral precancerous lesions, oral squamous cell carcinomas, and outcomea preliminary study

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    目的:研究p53 及 PTTG1 在口腔病變從正常口腔黏膜、癌前病變到口腔癌的表現及預後角色的相關性初步探討法:收集臺大醫院耳鼻喉科及口腔外科在1995年到 2001年的病人病理切片,共有141例,包括尚未接受治療之口腔癌前病變82例,及沒有遠隔轉移的口腔癌患者43例當做病患組,另選取2005年之正常的口腔黏膜病理切片16例,當做非病患組。採用石蠟包埋切片,做p53及PTTG1兩項生物標記的免疫組織染色,並定量此兩項生物標記在表皮細胞或腫瘤細胞染色表現的比例(Labeling indices, LI)。病人之資料收集採病歷回顧方式,記錄抽菸、喝酒、嚼檳榔等危險因子,及至2008年五月前所登錄,包括癌前病變病人轉變成口腔癌,或口腔癌病人術後的復發。死亡資料是以病人ID與國家死亡登錄資料庫碰檔取得。比較三組切片p53 與 PTTG1 LI之差異,並用線性回歸控制年齡、性別、生活型態等干擾因子。以原始之p53 與 PTTG1 LI值探討與癌前病變轉變為口腔癌,及口腔癌術後復發或存活之相關。在癌前病變轉變為口腔癌之p53 與 PTTG1之LI值,以ROC (Receiver operating characteristic) curve方法,選取最高的工具敏感度與特異性總和之最高值為切點,分成高LI與低LI組進行相關性分析。進一步以Cox 回歸模式及Kaplan-Meier curves計算兩組轉化為癌症之Hazard ratio,並做差異之檢定。本研究獲得台大醫院倫理委員會的同意。果:比較正常的口腔黏膜、口腔癌前病變及口腔癌之p53及PTTG1 LI值之差異; 發現兩種生物標記都會隨著口腔病變的嚴重程度而過度表現(over-expression), p53 LI值之呈現在正常口腔黏膜為0,癌前病變為2.20±0.71,口腔癌的表現為23.40±5.43, 其差異有統計上之意義(p=0.0001); PTTG1 LI值之呈現在正常口腔黏膜、癌前病變及口腔癌分別是32.5±9.05, 68.20±3.20與85.46±2.68其差異同樣有統計上之意義(p=0.0001); 在控制可能的干擾因子後,仍有意義的過度表現之差異。82名癌前病變病人在3到71個月的追蹤期間,其中有20名有口腔癌轉變,Cox 回歸模式評估癌前病變病人的口腔癌轉變,發現PTTG1 LI的表現可能與口腔癌轉變有關,其Hazard ratio 為 1.03 (1.00~1.05); 以PTTG1 LI值80%,分成高值組與低值組兩組,評估癌前病變病人的口腔癌轉變,進行Cox 回歸模式多變項分析,高值組的Hazard Ratio為4.70(1.29-7.60), 有統計之差異( p=0.019)。口腔癌的復發及存活情形,與兩種生物標記之 LI值,並無明顯相關。論:p53 及PTTG1 LI值在癌化的過程會隨著口腔病變的嚴重而過度表現。 PTTG1是癌前病變病人口腔癌轉變的獨立預後因子,可能可以用來當做預測口腔癌前病變轉變為口腔癌的預後因子。Purpose:he aim of this study is to explore the expression of two molecular markers (p53 & PTTG1) in oral cancer tumorgenesis and to explore their association with the prognosis of patients with oral precancerous lesion and oral cancer.ethods:ne hundred and forty one cases of formalin-fixed, paraffin-embedded specimens were collected and classified as patients group, including primary oral precancerous lesions (n=82) and squamous cell carinomas without distant metastasis (n=43). These patients received operation at the Department of Otolaryngology or Oral and Maxillofacial Surgery in NTUH during 1995-2001. On the other hand, sixteen specimens of normal oral mucosa were obtained during extraction of impacted permanent mandibular tooth in 2005 and classified as non-patients group. The expression of two biomarkers, p53 and PTTG1 in epithelial cells and cancer cells was measured with immunohistochemical staining and scored as labeling indices (LI). Patients’ clinicopathological parameters were retrieved from hospital records, including habits of alcohol smoking, betel nut chewing and cigarette smoking and the record of malignant development in precancerous lesions, cancer recurrence till May 2008. Mortality data was obtained from national death registry database. The expression of p53 and PTTG1 LI in normal oral mucosa, precancerous lesions and cancer were compared and adjusted with age, gender and lifestyle in linear regression. We analyzed the relation of initial p53 and PTTG1 LI with cancer development in precancerous lesions and recurrence or survival in oral cancers. The significance of p53 and PTTG1 LI in precancerous lesion with subsequent cancer development was determined in receiver operating characteristic (ROC) curve method. The point at which (sensitivity + specificity ) is maximized on the curve is taken as the best cut-off point and classified into two groups. Cox regression and time to event analysis with Kaplan-Meier curves method were used to compare the hazard ratio and determine the significant difference of these two groups in cancer development in precancerous lesions. This study was approved by the IRB of the NTUH.esults:he difference of p53 and PTTG1 LI in normal oral mucosa, precancerous lesions and cancers were compared; the expression of these two biomarkers over-expressed with the progression of severity of oral lesions. The p53 LI was 0 in normal oral mucosa, 2.20±0.71 in precancerous lesions and 23.40±5.43 in oral cancer, the difference was significant(p=0.0001). The PTTG1 LI was also significantly different and was 32.50±9.05, 68.2±9.1 and 85.5±2.68 respectively for normal oral mucosa, precancerous lesions and cancer (p=0.0001). After adjusting possible confounding factors, the expression of p53 and PTTG1 still showed a significant increase with the progression of oral epithelial lesions. Twenty patients in 82 oral precancerous lesions had malignant development during follow-up period from 3 to 71 months. The PTTG1 LI was significantly associated with cancer development in precancerous lesions in Cox regression model (Hazard ratio=1.03, 1.00~1.05); PTTGI LI ≧80% had the maximum sensitivity and specificity in predicting malignant development in precancerous lesions. The precancerous lesions were classified as high PTTG1 LI (≧80%) and low PTTG1 LI. The high PTTG1 LI was significantly associated with malignant development in precancerous lesions in multivariate Cox regression analysis (Hazard ratio=4.70, 1.29~7.60, p=0.019). The cancer recurrence and mortality were not associated with these two biomarkers.onclusion:TTG1 and p53 LI increased from normal oral mucosa to oral precancerous lesions and further increased in oral cancers. PTTG1 LI was an independent prognostic factor in predicting cancer development when oral precancerous lesions occurred. PTTG1 may be a potential prognostic marker in oral precancerous lesions.中文摘要…………………………………………………………………………….i-iibstract………………………………………………………………………..........iii-vontents…………………………………………………………………………..vi-viiiigures...........................................................................................................................ixables.........................................................................................................................x-xi. Introduction: rationale of this study……………………………………………1. Literature Review: ………………………………………………………………2.1 Commonly used prognostic factors in oral precancerous lesion and oral cancer………………………………………………………………………2.2 Molecular alterations in oral cancer nature history………………………4.3 Expression and prognostic value of p53 and PTTG1 in various tumors……5.3.1 Expression of p53 in normal oral mucosa, oral precancerous lesions and oral squamous cell carcinoma…………………………………………………5.3.2 Prognostic value of p53 expression in oral precancerous lesions……………………9.3.3 Prognostic value of p53 expression in oral squamous cell carcinoma…12.3.4 Expression of PTTG1’s and prognostic values in various tumors……13. Aims of this study………………………………………………………………17. Materials and Methods:…………………………………………………………18.1 Specimen collection of oral lesions………… …………………………18.2 Tissue processing, measurement of p53 and PTTG1 expression…………19 .3 Obtain the clinical data and subsequent pathology report with rectrospective medical chart review………………………………………………………21.4 Cancer development and mortality data……………………………………22.5 Statistical analysis…………………………………………………………23. Results……………………………………………………………………………26.1 The expression of p53 and PTTG1 in normal oral mucosa, precancerous lesion and oral squamous cell carcinoma: descriptive analysis of cross-sectional data…… …………………………………………………………………………………26.2 Correlation between p53 and PTTG1 expression in the same specimen………28.3 Univariate analysis of risk factors and expression of p53 & PTTG1 in precancerous and cancer lesions………………………………………………28.4 Risk factors adjusted p53 and PTTG1 labeling indices analysis………………29.5 Follow-up study of patients with precancerous lesions…………………………30.5.1 Cox regression analysis of the risk factors in oral precancerous lesions with subsequent cancer development……………………………………………30.5.2 Receiver operating characteristic (ROC) curve method for best cut-off point selection………………………………………………………………………31.5.3 KM method in oral precancerous lesions with subsequently malignant development analysis……………………………………………………………32.5.4 Univariate analysis with COX regression of PTTG1 and p53 in oral precancerous lesion and subsequently malignant development ………………33.5.5 Multivariate COX regression in oral precancerous lesion cancer development………………………………………………………………33.6 Follow-up study of patients with cancerous lesions…………………………34.6.1 Cox regression analysis of the correlation between local recurrence and risk factors, molecular markers…………………………………………………34.6.2 Time to event analysis with K-M method and Log-Rank test in oral cancer local recurrence analysis………………………………………………………35.6.3 Cox regression analysis of the correlation between overall survival and risk factors, molecular markers …………………………………………………35.6.4 Time to event analysis with K-M method and Log-Rank test in overall survival analysis………………………………………………………………36. Discussion…………………………………………………………………………37. Conclusion………………………………………………………………………40. References…………………………………………………………………………41iguresigure 2.1 Molecular progression model in oral cancer carcinogenesis......................46igure 4.1 Example of measurement of p53 expression in different severity of oral lesions………………………………………………………………………………47igure 4.2 Example of measurement of PTTG1 expression in different severity of oral lesions…………………………………………………………………………………48igure 5.1 Scatter plot showing the expression of p53 (A) and PTTG1 (B) from normal oral mucosa, different degree of precancerous lesions and oral cancer………49igure 5.2 The expression of p53 (A) and PTTG1 (B) in different degrees of precancerous lesions with epithelial dysplasia………………………………………49igure 5.3 Correlation between p53 and PTTG1 labeling indices in 141 specimens..50igure 5.4 ROC for PTTG1 & p53 LI in predicting oral precancerous lesion with subsequent cancer development………………………………………………………50igure 5.5 Kaplan-Meier curve for cancer free proportions…………………………52igure 5.6 Kaplan-Meier curve for local regional recurrence………………………54igure 5.7 Kaplan-Meier curve for overall survival in cancer patients………………56ablesable 2.1 Pooled prevalence estimate for p53 overexpression among normal oral mucosa (NOM), oral precancerous lesion (OPL) and oral squamous cell carcinoma (OSCC)………………………………………………………………………………57able 2.2 Meta-analysis for the expression of p53 in nature history of oral cancer....57able 4.1 Demography and life style data of study cases……………………………58able 4.2 Clinicopathologic features of oral precancerous lesion……………………58able 4.3 Characteristics of cancer stage and pathologic features……………………59able 5.1 Mean p53 and PTTG1 expression labeling indices (LI) in normal, precancerous and malignant oral mucosa……………………………………………60able 5.2 Relationship of p53, PTTG1 expression and different severity in oral cancer patients………………………………………………………………………………60ables 5.3 Correlation between p53 and PTTG1 expression in the same specimens……………………………………………………………………………61able 5.4 Univariate analysis of risk factors and p53 & PTTG1 expression in oral precancerous lesion……………………………………………………………………61able 5.5 Univariate analysis of risk factors and p53 & PTTG1 expression in cancer patients……………………………………………………………………………62able 5.6 Estimated parameters in linear regression model for p53 and PTTG1 labeling indices………………………………………………………………………63able 5.7 Correlation of p53 and PTTG1 initial labeling indices and subsequent cancer development in patients with precancerous lesion……………………………64able 5.8 Cox regression analysis in comparison of risk factors and cancer development…………………………………………………………………………64able 5.9 Comparison of different cut-off point of PTTG1 LI in predicting cancer development………………………………………………………………………65able 5.10 Cox univariate analysis in oral precancerous lesion with subsequent malignant development, with category data…………………………………………65able 5.11 Age adjusted and multivariate-adjusted Cox regression in oral precancerous lesion cancer development……………………………………………65able 5.12 Factors related to local regional recurrence—analysis with univariable Cox regression with continuous variable (p53 LI and PTTG1 LI)…………………………66able 5.13 Factors related to overall survival in oral cancer patients—analysis with univariable Cox regression……………………………………………………………6

    Dan jin shu yu shuang jin shu na mi jing ti cai liao: he cheng ji biao mian deng li zi ti gong zhen te xing

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    Li, Qian = 單金屬與雙金屬納米晶體材料 : 合成及表面等離子體共振特性 / 李倩.Thesis Ph.D. Chinese University of Hong Kong 2014.Includes bibliographical references.Abstracts also in Chinese.Title from PDF title page (viewed on 20, September, 2016).Li, Qian = Dan jin shu yu shuang jin shu na mi jing ti cai liao : he cheng ji biao mian deng li zi ti gong zhen te xing / Li Qian

    On the Exact Interval Estimation for the Difference in Paired Areas under ROC Curves

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    The GPQ-based method can be directly applied to evaluate the equivalence or non-inferiority of the newly diagnostic devices Research has been undertaken for construct the exact CI for the difference of the paired partial areas under the RO

    Effect of thermally aged oil on space charge dynamics in oil/paper insulation system

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    The formation of space charge in oil/paper insulation system can lead to material degradation in the high electrical field region and affect system reliability. Therefore, it is important to understand factors that affect space charge formation in oil/paper insulation system. In the present study the effect of thermally aged oil on space charge dynamics in oil/paper insulation system has been investigated using the pulsed electroacoustic (PEA) technique under different dc electrical fields at room temperature. The condition of oil was characterised. The ultraviolet/visible (UV/Vis) spectrum of oil shifts to visible wavelength and the oil acidity increased as the ageing time increased. It has been found that oil property has a significant effect on the space charge distribution of oil/paper insulation system. The more the deterioration of the oil and the higher the applied voltage, the larger the amount of negative charge injected into the paper near to the cathode and the positive charge accumulated at the paperpaper interface near to the cathode. The maximum electric field strength for oil/paper sample with seriously aged oil under 4kV and 6kV is more than 20% higher than its average electric field strength

    Hylomesa punctata Liao, Chen & Li 2022, sp. nov.

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    Hylomesa punctata Liao, Chen & Li, sp. nov. (Figs 1–8) Material examined. Holotype, ♀, China, Yunnan Province, Wenshan City, Malipo, 23°7′30″N, 104°42′7.19″E, 1124 m, V.2017, Yanqiong Peng (CNU); paratype, 1♀, China, Tibet, Linzhi City, Motuo County, Motuo Town, 29°19′30.97″N, 95°19′44.42″E, 1100 m, 21.V.1980, Gentao Jin & Jianyi Wu (CNU). Diagnosis. This species can be easily distinguished from all other members of the genus by the following character combination: transverse head (Fig. 3) shape, length from antennal insertion to occiput 0.86× width across eyes; surface of vertex close to occipital carina with very sparse punctures and largely smooth; punctures on dorsum of propodeum (Fig. 6) denser and more irregular; dorsum of propodeum with a broadly median groove. Description. Female. (Fig. 1). Body length 23.0– 23.1 mm, fore wing length 13.3–13.4 mm. Body almost black; mandible (Fig. 2) with a small area dark red (another specimen almost wholly reddish except black apex), and spines of legs more or less brownish. Wings strongly infuscate with weakly purple luster except hind wing basally. Head. Head (Fig. 3) transverse in dorsal view, length from antennal insertion to occiput 0.86× width across eyes; median lobe of clypeus (Fig. 2) narrowly emarginated apically, with indistinctly longitudinal median carina; frons (Figs 2, 3) with shallow median groove reaching anterior ocellus, lower half with coarse and dense punctures, upper half with relatively sparser punctures; OOD 1.27× POD and 0.45× OCD (Fig. 3), surrounding area of ocelli with coarse and dense punctures; vertex (Fig. 3) close to posterior area of hind ocellus with dense punctures, close to occipital carina with much sparser punctures than those of frons and largely smooth, anterior ocellus closer to apex of antennal tubercle than to occiput. Mesosoma. Pronotal transverse raised carina strongly present (Fig. 4), median length of pronotum 0.49× width of anterior margin and coarsely densely punctate, anterior two-thirds of dorsum with a few dense punctures, posteriorly with comparatively sparser and smaller punctures; lateral side (Fig. 5) of pronotum ventrally with densely striate; mesoscutum anteriorly impunctate, posteriorly with dense punctures especially in the middle; scutellum densely to moderately punctate; metanotum with dense punctures, smaller than those of scutellum; dorsal surface of propodeum (Fig. 6) with broad median groove containing transverse short striae, groove nail-shaped and base much wider than apex, the groove on each side distinctly margined with a carina, close to the carina with dense and variable sized punctures, and laterally with densely coarse punctures but larger and more irregular than the former, dorsum with bordering carina between horizontal and posterior surfaces; lateral surface of propodeum (Fig. 5) wholly with dense and oblique striae; ventral surface of hind femur medially with obtuse and short prominence. Metasoma. Length of T1 (Fig. 7) 0.71× maximal width and anteriorly with strong transverse carina, behind the carina with dense punctures (some contiguous), largely with sparse punctures, and posteriorly with a row of minute punctures (some contiguous) forming a transverse shallow subapical groove; S1 with basally transverse depression; T2–T5 with small and sparse punctures and subapically with a row of minute punctures; S2–S5 with sparse and small punctures and punctures on lateral surface slightly larger and denser; S6 with minute punctures; T6 (Fig. 8) anteriorly with moderate minute punctures, medially with sparser, deeper and larger punctures, apically impunctate and coriaceous. Male. Unknown. Distribution. China (Tibet, Yunnan). Etymology. The specific name is derived from the Latin word: punctata (= punctured), referring to dorsum of propodeum and vertex anteriorly with dense punctures.Published as part of Liao, Xiang-Ping, Chen, Bin & Li, Ting-Jing, 2022, A taxonomic revision of the subfamily Myzininae from China, with a key to the Chinese species (Hymenoptera: Tiphiidae), pp. 152-174 in Zootaxa 5154 (2) on page 155, DOI: 10.11646/zootaxa.5154.2.3, http://zenodo.org/record/664131
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